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Biomedical subjects

J J Collins

Publications and source records attributed to J J Collins.

At least 271 records · Page 15Linked to original sources
PubMed1981

Preservation of platelets and their function in prolonged cardiopulmonary bypass using prostacyclin.

The effects of prostacyclin (PGI2) with and without heparin were studied in 28 dogs that underwent 2 hours of cardiopulmonary bypass. Five groups were created: group I (six dogs) received heparin, 1.25 mg/kg; group II (six dogs) received low-dose heparin, 0.5 mg/kg, and PGI2, 500 ng/kg/min; group III (six dogs) received low-dose heparin alone; group IV (four dogs) received PGI2, 500--1000 ng/kg/min; and group V (six dogs) received ibuprofen, 12.5 mg/kg, dipyridamole, 1 mg/kg, PGI2, 20 ng/kg/min, and low-dose heparin. Significant clot deposition occurred in the oxygenators in groups III, IV and V. Platelet counts decreased to a mean of 36.8 +/- 5.7% (+/- SEM) of control in group I, which had normal clinical heparin dose for dogs, but to only 74 +/- 7% of control in group II. This improvement was significant (p less than 0.005). Platelet aggregation induced by adenosine diphosphate 60 minutes after CPB showed poor aggregation in group I but almost normal aggregation in group II. Protamine was unnecessary in groups that received PGI2. PGI2 in combination with low-dose heparin provides adequate anticoagulation during cardiopulmonary bypass in dogs, preserves platelet number and function and is associated with minimal postoperative bleeding.

Animals↗
PubMed1981

Emergency coronary revascularization.

Emergency operations for restoration of coronary artery blood flow are an effective means for treatment of unstable anginal syndromes. The risk of such operations is minimized by preoperative stabilization with medical therapy. Mechanical circulatory assistance may be a useful adjunct in some patients, especially in the presence of left main coronary obstruction. Utilization of emergency revascularization for patients with evolving myocardial infarction may be beneficial in some patients, but this approach remains controversial at present. Emergency revascularization for cardiogenic shock improves chances for survival in selected patients, and it may be combined with valve replacement, infarct resection, or repair of ruptured myocardium in patients with adequate residual contractile tissue.

Actuarial Analysis↗
PubMed1981

Immunologic control of the ascites form of murine adenocarcinoma 755. IV. Characterization of the protective antibody in hyperimmune serum.

The potent capacity of B6 anti-AD755a tumor cell serum to protect mice against challenge with large doses of the homologous tumor cells has been shown to reside in the IgG2a antibody subclass. Despite their inability to protect in vivo, other IgG subclass antibodies obtained from the anti-AD755a serum demonstrated serologic reactivities in vitro comparable to those obtained with the protective IgG2a fraction. The specificity of serum protection is linked to the oncornavirus associated with the AD755a tumor and the serum immunoprecipitates only virus structural proteins from the tumor cell surface. Removal of these antibodies by specific immunoadsorbent resins eliminated nearly all of the in vitro serologic reactivity of unfractionated serum and the IgG2a subclass, but it had absolutely no effect on their protective capacity in vivo. Further target cell-binding studies suggest that nonprotective antibodies in the anti-AD755a serum bind more efficiently to the target cell in vitro than the protective fraction and have raised the possibility that the latter antibodies may only have weak affinity for the target cell itself.

Animals↗
PubMed1981

Immunologic control of the ascites form of murine adenocarcinoma 755. V. Antibody-directed macrophages mediate tumor cell destruction.

An in vitro assay has been developed that mimics the potent in vivo protective capacity of B6 anti-AD755a serum in a passive therapy protocol. In the presence of small volumes of hyperimmune serum or IgG2a antibody, thioglycollate-elicited B6 mouse peritoneal cells (PEC) inhibit the growth of AD755 Cl.10 target cells and other cells provided that they express FLV-related antigens. When hyperimmune serum is replaced by normal serum, or elicited PEC from BALB/c mice are used, growth inhibition of the AD755 Cl.10 target cells is not seen. The latter is in accord with the inability to protect BALB/c mice with the anti-AD755a serum. Tumor cells to which antibody has been pre-bound are not inhibited by thioglycollate-elicited B6 PEC, analogous to the undiminished tumorigenicity of antibody-bound AD755a cells in vivo. These results, along with those presented in the accompanying papers, have led to the construction of a model to explain the specificity and mechanism of the potent in vivo passive protection characteristic of this system. The major features of this model are that the protective IgG2a antibody must first interact with an appropriate host effector cell, presumably of the monocyte/macrophage lineage, and that such an antibody-directed cell then binds to the tumor cell and effects its elimination, possibly by a phagocytic mechanism.

Animals↗
PubMed1981

The effect of low-dose aspirin and dipyridamole upon atherosclerosis in the rabbit.

To examine the effect of antiplatelet therapy upon atherosclerosis in an animal model, aspirin and dipyridamole were administered to female New Zealand rabbits while they were fed a 2% cholesterol diet. Four experimental groups of 15 animals were established: Group I (Control), no medication; Group II, aspirin, 40 mg orally five days a week; Group III, dipyridamole, 25 mg orally five days a week; Group IV, aspirin and dipyridamole. After seven weeks, the animals were sacrificed and their aortas were removed and stained. Group means of the percentage of total aortic lumenal surface occupied by gross atheromata were calculated and statistically compared with the control group mean: Group I - 49%, Group II 36%, p = NS, Group III - 47%, Group IV - 25%, p less than .01. Histologic sections of each aorta confirmed the stained areas to be atheromata of varying complexity. The lesions in animals treated with dipyridamole alone exhibited a distinct increase in smooth muscle cell proliferation. For animals receiving a combination of aspirin and dipyridamole the lesions were smaller and less advanced than those in the control group. These findings indicate that experimental atherosclerosis in rabbits is modified by the administration of anti-platelet agents and that atheroma formation is significantly inhibited when aspirin and dipyridamole are given in combination.

Animals↗
PubMed1980

Primary myxomatous degeneration of cardiac valves. Clinical, pathological, haemodynamic, and echocardiographic profile.

Four hundred and ninety-nine surgically excised valves were examined for pathological evidence of myxomatous degeneration. Thirty-six valves (7%) had myxomatous degeneration as a major pathological finding. Fourteen valves (3%) had significant myxomatous degeneration of the pars fibrosa, a finding which we define as "primary myxomatous degeneration". Echocardiographic findings and catheterisation results were correlated with the clinical course, surgical results, and follow-up in these 14 patients. Echocardiograms in 10 of the 11 patients who had them (91%) showed abnormalities suggesting the presence of primary myxomatous degeneration. Echocardiography was more helpful than angiography in diagnosis. The histological pattern of primary mitral myxomatous degeneration appears to be identical to that seen in patients with mitral valve prolapse and five of six patients with mitral lesions had echocardiographic evidence of prolapse. None of the patients with primary myxomatous degeneration of the aortic valve had syphilis of Marfan's syndrome. While the aetiology of primary myxomatous degeneration of cardiac valves is not known, a link to a more generalised disorder is suggested.

Adult↗
PubMed1980

Absence of macrophage involvement in the passive serum therapy of Friend leukemia virus-induced disease.

The possible involvement of host macrophages in the passive serum therapy of Friend leukemia virus (FLV)-induced disease has been examined with the use of agents inhibiting normal macrophage functions, including silica and a tumor-produced macrophage chemotaxis inhibitor. Under conditions in which macrophage chemotaxis inhibitor. Under conditions in which macrophage functions are at least transiently abrogated by these agents, no effect was seen on the anti-fLV protection afforded by the passive administration of chimpanzee anti-FLV antiserum to infected DBA/2 mice, as monitored by the development of virus-induced splenomegaly and the level of infectious virus. The macrophage inhibitors also did not influence the appearance of the host antiviral humoral immune response which normally accompanies serum protection. These results suggest that the normal functioning of host macrophages do not play a central role in the passive serum therapy protective mechanism leading to resistance to FLV infection.

Animals↗
PubMed1980

Functional comparison of coronary bypass grafts of the saphenous vein and internal mammary artery.

The magnitude and distribution of myocardial blood flow through a saphenous vein (SV) bypass graft and an internal mammary artery (IMA) graft (diameter greater than or equal to 2 mm) into the same left anterior descending coronary artery (LAD) (diameter congruent to 1.5 mm) were determined at rest, with atrial pacing, and with elevated left ventricular end-diastolic pressure (LVEDP) in 18 dogs. Blood flows through the native LAD, SV, and IMA grafts were similar in the resting heart. With atrial pacing (heart rate = 150% of control), flow in both the SV and IMA grafts increased but the difference was not significant. With elevated LVEDP (20 mm Hg) produced by transfusion, flow in both SV and IMA grafts increased, but, again, these increases were not significantly different. The SV and IMA bypass grafts have similar flow rates at rest and during increased functional demand, provided the grafts are larger than the vessels into which they are placed.

Animals↗
PubMed1979

Role of the spoT gene product and manganese ion in the metabolism of guanosine 5'-diphosphate 3'-diphosphate in Escherichia coli.

Addition of divalent ion chelating agents picolinic acid, 1,10-phenanthroline, or quinoline-2-carboxylic acid to wild type, relA, or relX, but not spoT strains of Escherichia coli increases the levels of guanosine 5'-diphosphate 3'-diphosphate (ppGpp). Poorly chelating analogs of these agents and a larger and more highly charged chelating agent, ethylene glycol bis(beta-amino-ethyl ether) N,N,N',N'-tetraacetic acid are ineffective. Mn2+ reverses the increase in ppGpp. The increase in ppGpp in wild type cells can be explained by an inhibition of degradation. In spoT cells the response is more complex; ppGpp does not increase although degradation is completely inhibited. The lack of increase in spoT cells suggests a role for spoT in synthesis of ppGpp in addition to its known role in degradation. Growth of both spoT+ and spoT cells is inhibited following chelator addition. This suggests that growth inhibition is through a mechanism not directly involving ppGpp. The results of this study provide evidence in intact cells for a role for Mn2+ and the spoT gene product in ppGpp degradation, and provide further evidence for an involvement of spoT and possibly divalent ions in ppGpp synthesis.

Alleles↗
PubMed1979

Transient growth inhibition of Escherichia coli K-12 by ion chelators: "in vivo" inhibition of ribonucleic acid synthesis.

The ion chelators picolinic acid, quinaldic acid, 1,10-phenanthroline, and 8-hydroxyquinoline, but not ethylenediaminetetraacetate, ethyleneglycol-bis-(beta-aminoethyl ether)-N,N-tetraacetate, or dipicolinic acid, rapidly but transiently arrest growth of Escherichia coli K-12. Cells adapt and become resistant to growth inhibition by these agents, a process which requires protein synthesis. Mn2+, at low concentrations, decreases the time required for resumption of growth. Proteins synthesized during the lag are quantitatively and qualitatively different from those synthesized during normal growth. Inhibition of growth can explained by an effect on RNA polymerase, a known metalloenzyme.

Adaptation, Physiological↗
PubMed1979

Long-term follow-up of the Hancock bioprosthetic heart valve: a 6-year review.

Clinical experience with the Hancock porcine bioprosthetic heart valve was reviewed in 467 patients (254 men and 213 women, 18--84 years old, average, 56 years) who received 528 valves from January, 1972, to January, 1978. Associated procedures, including coronary bypass graft, ascending aortic aneurysm, and valvuloplasty were done in 102 of the 467 patients (22%). The overall operative mortality was 25/467 (5.6%), 12/226 (5.3%) for aortic valve replacement (AVR), 11/183 (6%) for mitral valve replacement (MVR), and 2/58 (3.4%) for multiple valve replacement. The first 323 patients with a minimum follow-up of 16 months (16--75 months, average 33 months) were analyzed for survival and thromboemboli. Actuarial survival at 66--75 months was 75.7% for AVR, 79% for MVR, and 75.8% for multiple valve replacement. Emboli per 100 patient-years was 0.55 for AVR (no anticoagulants), 3.9 for MVR, and 4.8 for multiple valve replacement (anticoagulants for atrial fibrillation patients only); emboli occurred only in patients with atrial fibrillation. There were seven of 528 primary dysfunctional valves (1.3%): calcification in two, tissue failure in two, and fibrosis in three. A hemodynamic study of four patients with a 21 mm Hancock Modified Orifice aortic valve prosthesis showed improved orifice areas (greater than 1.3 cm2) over the standard aortic valve. The Hancock porcine xenograft bioprosthetic heart valve has been a durable heart valve in excess of 6 years and has a low associated incidence of thromboemboli in patients off anticoagulants except in those with chronic atrial fibrillation.

Adolescent↗